An unexpected link between these EEG studies and the genetic analysis of AUD identified a haplotype of a potassium channel subunit that not only mediates changes in excitability but is also itself regulated by ethanol, with increased levels causing a shift in metabolic flux. Genome-wide association studies for one of these AUD-associated EEG phenotypes - elevated theta ERO power - have identified multiple non-coding single nucleotide polymorphisms (SNPs) within the KCNJ6 gene in strong linkage disequilibrium (LD) (Kang et al., 2012). Individuals with this haplotype of KCNJ6 SNPs demonstrated increased theta ERO power and altered EEG topography during reward processing in a monetary gambling task, suggesting a genetic influence on neuronal function (Clarke et al., 2011, Kamarajan et al., 2017). KCNJ6 encodes the G protein-coupled inwardly rectifying potassium channel subunit 2 (GIRK2), which plays a key role in controlling neuronal excitability (Glaaser and Slesinger, 2015, Luscher and Slesinger, 2010, Zhao et al., 2021). Activation of inhibitory G protein coupled receptors (GPCRs) via ligand binding leads to GIRK2 activation via Gβγ, resulting in outward potassium flux through the channel and subsequent
